Childhood Onset Schizophrenia

Childhood Onset Schizophrenia (COS) is known to result in a more severe and debilitating form of schizophrenia. It is rare, but often studied, as researchers try to look at the factors that lead to the adult disease, focusing on the neurodevelopmental theory. They have looked at overall development of children born to parents who have schizophrenia. They have looked at the frequency of obstetrical complications in individuals with schizophrenia. They have looked at the brain development of those with COS as compared to adolescents and adults. In each area they find clues to the reasons behind this illness. It is fascinating to see how many early events have a part in the development of this disease.

Even before childhood, at birth these individuals seem to have factors that are part of their eventual development of schizophrenia. Cannon has postulated that obstetrical complications combined with genetic factors lead to schizophrenia. He has found that early onset schizophrenia (EOS) is 7.30 times more likely to have had hypoxic obstetrical complications than those with adult onset. This can contribute to the early brain lesion that researchers feel is ultimately behind the development of schizophrenia. Cannon also proposes that this earlier onset in COS allows for an earlier and more robust pruning of synapses during adolescence – “variations in the rate of synaptic pruning would vary the age of clinical onset of schizophrenia” (Cannon 2000).

In terms of development, there have been studies that look back at the early lives of people with schizophrenia to see if there are any early signs that might give a clue as to who will develop the disease. In interviewing parents, it has been found that those who go on to develop schizophrenia have delayed speech milestones, difficulty in reading and writing, and greater overall developmental deviance. They show poor premorbid adjustment in childhood. Particularly boys show even more as they move through adolescence. There are cognitive deficiencies and some motor difficulties. Finally, they show more Schizophrenia Spectrum trait (Hollis 1995). What’s particularly interesting is that they have found more impairment in COS than in even EOS. One study by Vourdes has shown a 19.4% delay in language and speech in COS as compared with EOS. They also found that schizophrenia spectrum traits were more pronounced in COS. They exhibited more deviance in bizarre ideas and perceptions, more of a restricted affect and odd speech (Vourdes 2003). Nicholson has found that there is a much higher incidence of PDD in children that go on to develop COS. 25% of those with COS had a premorbid PDD, showing a social impairment most predominantly, he reports that PDD in COS is more likely to be a marker of severe early abnormal neurodevelopment (Nicholson 2003). So, there are significant early markers for this illness. These could in fact lead to earlier diagnosis, before the devastating symptoms emerge and then maybe earlier treatment that might prevent some of the brain destruction.

Moving into the more specific changes that are found in the brains of adolescent and COS. Thompson took a cohort of COS and took 3 MRI’s at 2 year intervals to see the progression of brain changes between childhood through adolescence “Over 5 years, these deficits progressed anteriorly into temporal lobes, engulfing sensorimotor and dorsolateral prefrontal cortices, and frontal eye fields. These emerging patterns correlated with psychotic symptom severity and mirrored the neuromotor, auditory, visual search, and frontal executive impairments in the disease” (Thompson 2001). Researchers are trying to connect symptoms to brain areas and finding some correlations. This has been attempted over the years, but it seems they are finally finding some real connections. It was also found that in some areas of the brain the tissue loss was faster the younger the client was and that the faster there was tissue loss, the more severe the symptoms.
Coming at this from another angle – looking at the loss of grey matter in COS Gogtay compared COS with children with atypical psychosis. Gogstay suggests that there is a diagnostically specific GM volume loss in COS that was not seen in children with atypical psychosis. “An ongoing neurodevelopmental process and/or brain response specific to the illness could account for these changes.” (Gogtay 2004)
There are a number of factors that all seem to play into the development of schizophrenia from a very early age. Comparing the neurodevelopment of those with the more severe COS with those without yields much interesting data. (Rapoport 2004) It seems to point to an element – genetic – that is then compounded by environmental effects. The maturing brain then adapts to this maladaptation and develops in specific patterns the symptoms. The more we can learn about the early indicators of this illness, the closer we can get to the root causes. Interesting work is being done on looking at all these factors as they relate to the interconnectivity of the disorder. It is clearly not one gene or birth insult or developmental pattern. It is rather the interplay of all these factors that will lead into understanding more fully the causes and development of this devastating disease.

References
Thompson PM, Vidal C, Giedd JN, Gochman P, Blumenthal J & Nicolson R
et al.. Mapping adolescent brain change reveals dynamic wave of
accelerated gray matter loss in very early-onset schizophrenia.
Proc Natl Acad Sci USA 2001; 98: 11650−11655.

Cannon TD, Rosso IM, Hollister JM, Bearden CE, Sanchez LE & Hadley T.
A prospective cohort study of genetic and perinatal influences in
the etiology of schizophrenia. Schizophr Bull 2000; 26: 351−366.

Hollis C. Child and adolescent (juvenile onset) schizophrenia. A case
control study of premorbid developmental impairments. Br J
Psychiatry 1995; 166: 489−495.

Gogtay N, Sporn A, Clasen LS, Nugent TF, III, Greenstein D & Nicolson R
et al.. Comparison of progressive cortical gray matter loss in
childhood-onset schizophrenia with that in childhood-onset
atypical psychoses. Arch Gen Psychiatry 2004; 61: 17−22.

Vourdas A, Pipe R, Corrigall R & Frangou S. Increased developmental
deviance and premorbid dysfunction in early onset schizophrenia.
Schizophr Res 2003; 62:13−22.

Nicolson R, Brookner FB, Lenane M, Gochman P, Ingraham LJ & Egan MF
et al.. Parental schizophrenia spectrum disorders in childhood-
onset and adult-onset schizophrenia. Am J Psychiatry 2003; 160: \
490−495.

J L Rapoport1, A M Addington1, S Frangou2 and M R C Psych2 The
neurodevelopment model of schizophrenia: update 2005 Molecular
Psychiatry (2005) 10, 434–449.

5 thoughts on “Childhood Onset Schizophrenia

  1. This is a fascinating topic. I have frequently wondered if most (if not all) schizophrenia is childhood onset. Despite being a disorder identified more commonly in late adolescence/early adulthood, most of the patients with schizophrenia I have encountered reported an awareness of their symptoms far, far earlier than their first psychotic break. Though this is all anecdotal, many of them also reported having told an important adult (usually a parent), who dismissed them as just having “imaginary friends”, being a “difficult” or “challenging” child, or otherwise disruptive. These children learned how to mask their symptoms as needed in an effort to meet the needs of others around them. As your review of the research suggests, the progression of the disease in its march across the brain can be observed. I wonder if the initial psychotic breaks we see in the treatment realm are the result of a brain that can no longer contain the disease’s progression, and about which the patient may have long been aware. It would be interesting to see a study of a population of children over time, some of whom are statistically more likely to acquire the disorder, where both interview and brain scanning is used to identify the disease, to see its origins even earlier than the presentation of observable symptoms.

  2. Fascinating indeed! I’m wondering, given the early issues regarding speech, reading, writing, and motor delays, what affects early intervention to aid in supporting individuals with these issues would have on the neurological development and loss of gray matter. In other words, is there any way that we can prevent the unnecessary synaptic pruning and degeneration of various brain areas. This article gives some interesting background on some efforts (medication, CBT, family interventions), but also goes into some of the controversy of early diagnosis of prodromal syndromes and the effects it can have: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2738348/

  3. Childhood schizo is something that honestly really worries me as a provider. As I work with younger people, there are usually the same range of issues, most commonly ADHD. Schizo isn’t the first thing that comes to mind when evaluating a young patients. I have a patient that has genetic loading for Schizo and I wonder how many kids would come out tell a provider about the positive symptoms of Schizo. To me, i think kids would be more guarded.

  4. Learning about prodromal symptoms of schizophrenia has been something that I’ve been interested in as well. It is such a disabling mental illness and speaking with families of patients who have their first psychotic break in their twenties comes close to home because I struggle with picturing what my life would be like if this happened.

    I had a patient last year that came from an upper middle class white family. He had his first psychotic break at 23 and his auditory hallucinations were so disabling that for that past 3 years, he had been in and out of inpatient psychiatric hospitalizations. His command hallucinations made him believe that he needed to rip the veins out of his arms. Seeing him in the hospital was very sad and made me frustrated and think a lot about this patient’s trajectory. His command hallucinations were so strong and made him truly believe he needed to cut open his veins. In my eyes, and I’ve been struggling a lot thinking about this, but his chances of survival are potentially as low as a patient with cancer. While all of these studies and the research being done has come a long way, I become frustrated with the lack of research and resources dedicating to mental illnesses.

  5. Interesting and saddening at the same time. This is a subject I have always thought about. I have seen just one case of child onset Schiz back in Nigeria, and the boy was on 10years old. It was very strange to me because the general belief in my country is it is . impossible for a kid to be psychotic. I kept wondering about what could have been the cause. I saw the boy at the ED and since I was not directly involved in his care, I could not really get more information. This post although not absolute has shed more lights on my questions

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